Clinical application of cefoperazone/sulbactam combined with thymosin α1 for the treatment of severe pneumonia caused by Acinetobacter baumannii / 中国感染控制杂志

Objective To evaluate the clinical efficacy and prognosis of cefoperazone/sulbactam combined with thymosin α1 in the treatment of severe pneumonia caused by Acinetobacter baumannii (A.baumannii).Methods 84 patients with severe pneumonia caused by A.baumannii were randomly selected,they were divided into treatment group(n =42,cefoperazone/sulbactam combined with thymosin α1 treatment) and control group(n =42,only cefoperazone/ sulbactam treatment).Procalcitonin(PCT),C-reactive protein(CRP),white blood cell(WBC) count,peripheral blood T lymphocyte subsets,interleukin-6(IL-6),interleukin-10(IL-10),immunoglobulin G (IgG),and APACHE II score of two groups before treatment and 7 days after treatment were compared,ventilator weaning success rate,length of ICU stay,and 28-day mortality were also observed.Results After 7 day treatment,compared with the control group,CD4 + T cells,CD4 +/CD8 +,IL-10,and IgG in the treatment group were all significantly higher (all P＜0.05);PCT,CRP,WBC,IL-6,and APACHE II score all significantly declined,difference were all significant(all P＜0.05).Ventilator weaning success rate in treatment group was higher than control group (64.29％ vs 38.10％),mean length of ICU stay was shorter than control group([12.41-± 2.25]d vs[18.23 ±-2.50]d),28-day mortality was lower than control group(19.05％ vs 45.24％),difference were all significant(all P＜0.05).Conclusion Cefoperazone/sulbactam combined with thymosin α1 for the treatment of severe pneumonia caused by A.baumannii can improve the immune function of patients,reduce inflammation,increase ventilator weaning success rate,shorten ICU stay,and decrease 28 day mortality.

Correlation of restenosis after rabbit carotid endarterectomy and inflammatory cytokines

OBJECTIVE@#To establish rabbit model of restenosis after carotid endarterectomy surgery, and to study tissue inflammatory cytokines (TNF-α, IL-6) involved in restenosis.@*METHODS@#A total of 32 rabbits were randomly divided into two groups: model group and control group. The right common carotid artery in rabbits was damaged by carotid endar terectomy in model group. The tissues were harvested at different time points respectively, the pathological changes of the vascular wall after operation were observed at different time points. The changes of expression of tissue vascular wall inflammatory cytokines (TNF-α, IL-6) at different time points after the surgery was observed by RT-PCR, and the changes of serum inflammatory cytokines (TNF-α, IL -6) were detected by ELISA.@*RESULTS@#The new intima appeared after 7 days of the injury and reached the peak on 28 d which is uneven and significantly thicker than the control group (P<0.01). The tissue inflammatory cytokines (TNF-α, IL-6) were significantly increased after the rabbit common carotid artery injury, which was significant difference compared with normal control group (P<0.05).@*CONCLUSIONS@#The tissue inflammatory factors significantly increase after the rabbit carotid artery injury, which suggests the mutual concurrent effects of inflammatory cytokines can result in the proliferation of vascular restenosis.

Role of Ca2+/calmodulin-dependent calcineurin signaling pathway in neuropeptide Y-induced cardiac hypertrophy in rats / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the role of Ca(2+)/calmodulin-dependent calcineurin (CaN) signaling pathway in neuropeptide Y (NPY)-induced cardiomyocyte hypertrophy in rat.</p><p><b>METHODS</b>Cardiomyocytes of neonatal Wistar rats were cultured in the presence of 10 and 100 nmol/L NPY, and cyclosporine A (CsA) was applied to inhibit the activity of CaN. The protein synthesis rate, c-jun mRNA expression, CaN protein expression, CaN activity and intracellular Ca(2+) concentration in the cardiomyocytes were assessed.</p><p><b>RESULTS</b>Compared with the control group, (3)H-Leu incorporation and expression of c-jun mRNA in the cardiomyocytes treated with 100 nmol/L NPY increased significantly (P<0.05, P<0.001), and the effect of NPY was blocked by CsA. The activity of CaN (P<0.05), CaN expression (P<0.05), and Ca(2+) concentration in the cytoplasm (P<0.001) and nuclei (P<0.001) of the cells with 100 nmol/L NPY treatment also significantly increased compared with those in the control cells.</p><p><b>CONCLUSION</b>NPY can induce cardiomyocyte hypertrophy in rats, in which process Ca(2+)/calmodulin-dependent CaN signaling pathway plays an important role.</p>